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Problem Solving Exercises in Cardiovascular Physiology and Pathophysiology

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Problem Solving Exercises in Cardiovascular Physiology and Pathophysiology Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 Problem Solving Exercises in Cardiovascular Physiology and Pathophysiology Elapulli S. Prakash, MBBS, MD Division of Basic Medical Sciences, Mercer University School of Medicine Macon, GA, USA E-mail: [email protected] 1 Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 Some notes on terminology: Unless otherwise specified, the term BP refers to systemic arterial blood pressure obtained in the brachial artery held at the level of the heart, and mean arterial pressure refers to mean systemic arterial pressure. stroke volume, end-diastolic volume, end-diastolic pressure, and ejection fraction, refer to parameters of the left ventricle. systolic pressure, diastolic pressure, pulse pressure, mean arterial pressure all refer to pressures in the systemic arteries. Any other usage of these terms should be with appropriate qualifications; example, pulse pressure in pulmonary artery. 2 Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 Questions and Answers: 1. Does constriction of arterioles in finger flexors increase mean arterial pressure (MAP)? It may or it may not. Vasoconstriction in a tissue (i.e., an increase in Local Vascular Resistance, LVR) does not necessarily increase total peripheral resistance (TPR; aka. systemic vascular resistance (SVR). MAP is the product of SVR and cardiac output, and one cannot predict with certainty if a change in LVR in one tissue will TPR and or cardiac output. Vasoconstriction in certain tissues (example, coronary circulation), may elicits a reflex increase in sympathetic discharge. This may result in an increase in TPR. Myocardial ischemia, CNS ischemia, ischemia of metabolically active skeletal muscle, renal ischemia, are all known to elicit reflex increases in sympathetic discharge to resistance vessels that may result in a rise in MAP. Again one cannot predict with certainty; it is best to work backward to reason observations. 2. If the radii of all arterioles in a group of metabolically active forearm flexor muscles doubled, and the mean systemic arterial pressure increased by 50%, to what extent would you expect this to affect blood flow to these muscles assuming no change in viscosity of blood? The Poiseuille-Hagen equation summarizes the effect of various factors on mean resistance R as follows: R = 8ηL / πr4 where η - viscosity of blood; L - length of the vessel; r - radius of the vessel Thus, flow Q = ΔP / mean R = ΔPπr4 / 8ηL. This equation may be applied to characterize vessels that for practical purposes can be assumed to be rigid tubes with a steady flow rather than pulsatile flow. For the question posed an approximately 24 fold increase in blood flow to the muscles would be predicted. Observed values might depart from this prediction (10-20% either way). In general, as for the magnitude of hyperemia in rhythmically contracting muscle, there is evidence that it can increase as much as 30-fold from baseline. (Ganong, 2005, p. 632). 3. In the upright posture a considerable volume of blood pools in the veins of the lower limb because of the effect of gravity. Does blood normally ‘pool’ (to that extent) in the arteries of the lower limb? Veins are capacitance vessels and can readily accommodate more blood (of course within limits) relative to the low capacitance, high resistance, high pressure arterial system. Because of the limited compliance (relative to veins), blood does not really pool in the arteries to a significant extent unless there is tremendous arteriolar dilation. 4. In a healthy adult in the upright position, MAP in the brachial artery (at the level of the heart) was found to be 100 mm Hg. In this position, what would the MAP be in a cerebral artery 50 cm above the heart? What would the MAP be in an artery in the foot 100 cm below the heart? How would you expect blood flow to brain tissue 50 cm above the heart and tissue in the feet 100 cm below the heart to compare? Explain. The magnitude of the effect of gravity on hydrostatic pressure is 0.77 mm Hg/cm at the density of normal blood (there is no need to memorize this). It is important to note however that in an artery in the foot 100 cm below the heart, the mean hydrostatic pressure is 177 mmHg, whereas 3 Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 in an artery 50 cm above the heart, it is 62 mm Hg [i.e., 100 – (50 × 0.77)]. However, that gravity has a similar effect on hydrostatic pressure in veins. As a result, the driving pressure is not any different between an artery in the head and an artery in the foot even in the upright posture. Blood flow to a tissue equals driving pressure (perfusion pressure) divided by local vascular resistance. Moreover, flow is regulated by varying local vascular resistance. The point of the question is to exemplify the distinction between driving pressure and hydrostatic pressure. When we talk about BP, we refer to the driving pressure; everywhere in the systemic arteries it is normally the same and it is simply considered to be the MAP at the level of the heart. If the question is whether gravity has an effect on the absolute value of driving pressure (blood pressure), the answer is it may as a result of the reduction in venous return associated with upright posture. 5. During exercise, a healthy 30-year-old male with no evidence of cardiac shunts consumes 2 liters of oxygen per minute. His brachial artery O2 content is 200 ml/L and the oxygen concentration of mixed venous blood obtained from the pulmonary artery is 100 ml/L. What is his cardiac output? Fick’s principle states that the amount of a substance consumed by an organ per unit time (A) = A-V conc. difference of that substance × blood flow through that organ or vascular bed. Thus, blood flow (Q) = Amt. of the substance consumed / A-V concentration difference for that substance Fick principle is an application of the law of conservation of mass. For cardiac output estimation, O2 uptake by the lungs which equals oxygen utilization by systemic tissues has been used as the indicator substance. O2 consumption = 2 L/min = 2000 ml/min. Systemic arterial O2 = 200 ml/L. Since there are no shunts, pulmonary artery blood represents fully mixed systemic venous blood, and its oxygen concentration is 100 ml/L. Thus, cardiac output = 2000 / (200- 100) = 20 L/min. 6. In a 6-year-old child with tetralogy of Fallot, the hematocrit was observed to be 60. What is its likely impact on ventricular afterload? An increase in hematocrit from 35 to 50 does not increase viscosity appreciably but increases oxygen carrying capacity of blood considerably. Whereas, an increase in Hct from 40 to 60 doubles viscosity of blood effectively doubling vascular resistance and consequently the load on the heart, and this partly offsets advantages accruing from an increase in oxygen carrying capacity of blood to some extent. (See Boron, p. 457, Fig 18-8). 7. Thin walled capillaries do not burst when they are exposed to a pressure as high as 40 mm Hg. How can this be explained? For a thin walled structure like a capillary, Laplace’s law is written as P = T/r where P is distending pressure, where T is wall tension and r is the radius. (Boron pp. 476-477). The distending pressure of blood in the capillary stretches the capillary increasing the passive tension in its wall. Because of its small radius (5 microns), the amount of passive tension needed to 4 Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 withstand the pressures it is normally exposed to it is small. In contrast, the aorta is exposed to a pressure of about 120 mm Hg with every heartbeat. To withstand this distending pressure, the aortic wall tension is about 1000 times greater, and the aorta is much thicker. In this regard, arterioles have a very important function; if it were not for the relatively high resistance of arterioles, much higher pressures would be transmitted to capillaries. 8. Examine this EKG. Calibration is standard (10 mm = 1 mV, and speed is 25 mm/s). What is the heart rate and rhythm? Source: ECGpedia. http://en.ecgpedia.org/wiki/File:Nsr.jpg Creative Commons Attribution- Share Alike 3.0 Unported license; accessed Sep 12, 2013. RR intervals are fairly regular and the HR averages approximately 75 bpm. Regarding rhythm, analysis of rhythm can be broken into two parts: Is this sinus rhythm? If the rhythm is sinus, the impulse exciting the ventricle originated in the SA node. If it is not sinus rhythm, then what is the rhythm? The 12 lead EKG along with a rhythm strip should be examined for this: P wave is upright in lead II and inverted in aVR, or P should be upright in leads I, II and III. Each P wave is followed by a QRS complex Every QRS complex is preceded by a P wave PR interval is normal. 5 Prakash ES. Problem Solving Exercises in Cardiovascular Physiology & Pathophysiology. Revised July 2014 QRS duration is normal. QRS rate is between 60-100 bpm. (Some build in this criterion and consider sinus tachycardia and sinus bradycardia as arrhythmias. Some consider sinus bradycardia and sinus tachycardia simply as abnormalities of rate rather than rhythm.) Additionally, if checked, RR interval length may be seen to vary with the phase of breathing (see below). The positive terminal of lead II corresponds to + 60 degrees in the hexaxial reference system.
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